When a gene is beneficial to one sex, but harmful to another, it is referred to as sexually antagonistic and it is theorized that molecular solutions ar in place to alleviate the conflicting selection pressures to optimize the fitness of each sex. Preliminary results revealed a high proportion of newly evolved genes in Drosophila melanogaster are sexually antagonistic for reproductive fitness compared to the whole genome average, suggesting for the first time new genes are a genetic basis for sexual antagonism in Drosophila melanogaster. This observation immediately provoked significant scientific questions: What is the relationship between sexual antagonism evolution and gene age? Is sex biased expression a mechanism to resolve sexual antagonism? To address these questions, Aim 1 will identify sexually antagonistic genes through fitness analyses of genes in different age groups. RNAi technology will be used to knockdown the expression of Drosophila melanogaster genes from three age groups, 1-6 million years (MY), 6-25 MY, and >35 MY, and male fertilization success and female fecundity will be quantified by comparing the number of resulting offspring in the gene knockdown crosses to parallel control crosses. This data will be used to identify the proportion of sexually antagonistic genes across the three age groups and determine if a greater proportion of young genes are sexually antagonistic compared to ancient genes in regards to reproductive fitness.
Aim 2 will discover the sex bias tendencies of sexually antagonistic genes of varying ages. Custom reproductive structure and gamete transcriptome data, gene-specific QPCR expression data, and publicly available expression data will be utilized to determine the sex-biased and tissue specific expression of the genes across the three age groups. The results of this study will provide experimental evidence to either support or reject the theories pertaining to sex-biased expression being a mechanism for sexual antagonism resolution. A model of sexual antagonism evolution will be developed through this project, which can be applied across species and can be used to predict the evolutionary trajectory of key fitness genes. The results of this project will introduce a new method for identifying sexually antagonistic genes involved in human sexual dimorphic traits, by using gene age as an indicator, which may lead to the identification of central genes involved in human fertility and secondary sex characteristics for future study.
I propose to investigate how newly originated genes drive the evolution of sexual antagonism in Drosophila melanogaster, to understand if this intralocus sexual conflict, which occurs when a single gene is beneficial to one sex, but harmful to the other sex, can resolve over evolutionary time through sex-biased gene expression. This study will experimentally test theoretical hypotheses about the evolution of the genetics underlying phenotypic differences between males and females, to gain a fundamental understanding of the evolutionary trajectory of important fitness genes across species. A model of sexual antagonism evolution will be developed through this project, providing a new and valuable method for identifying genes important in reproduction and secondary sexual characteristics for future medical studies.
